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Neurochem Res. 2018 Sep;43(9):1736-1744. doi: 10.1007/s11064-018-2589-5. Epub 2018 Jun 30.

Neohesperidin Prevents Aβ25-35-Induced Apoptosis in Primary Cultured Hippocampal Neurons by Blocking the S-Nitrosylation of Protein-Disulphide Isomerase.

Author information

1
Department of Medicine, Xi'an Jiaotong University, No. 76 Yanta West Road, Yanta District, Xi'an, 710061, China.
2
Shaanxi Province People's Hospital, No. 256 Youyi West Road, Yanta District, Xi'an, 710068, China.
3
Department of Medicine, Xi'an Jiaotong University, No. 76 Yanta West Road, Yanta District, Xi'an, 710061, China. zhangylzhyl@126.com.
4
Shaanxi Province People's Hospital, No. 256 Youyi West Road, Yanta District, Xi'an, 710068, China. zhangylzhyl@126.com.

Abstract

A growing body of literature has established a link between the cerebral ischaemic injury and pathological state of Alzheimer's disease (AD), and this correlation indicated that the preventive agent for ischaemia might improve the pathology of AD. Our previous studies have demonstrated that Neohesperidin (NH) exhibited neuroprotective effects against cerebral ischemia via the down-regulation of Bcl-2, Akt/PI3K and Nrf2 pathways. In the present study, we first confirmed the protective effects of NH on Aβ25-35-induced neurotoxicity on primary cultured hippocampal neurons. We further demonstrated NH attenuated Aβ25-35-induced apoptosis by preventing neurotoxicity associated with lethal UPR and ER stress via blocking S-nitrosylation of protein-disulphide isomerase (PDI). These results suggested that S-nitrosylation of PDI and ER dysfunction might be the synergistic and synchronous pathological process between cerebral ischaemia and AD.

KEYWORDS:

Aβ25–35; ER stress; Neohesperidin; PDI; S-Nitrosylation

PMID:
29961232
DOI:
10.1007/s11064-018-2589-5
[Indexed for MEDLINE]

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